The Kinesin Motor Kif9 Disrupts Primary Cilia Length by Mispositioning Centriolar Satellites

Abstract

Primary cilia are nonmotile, microtubule-based structures on the surface of most vertebrate cells, acting as sensory hubs to regulate cellular responses. Their formation, maintenance, and disassembly are tightly regulated, with dysfunction linked to diseases like ciliopathies, cancer, and neurological disorders. Centriolar satellites (CS), membrane-less granules around the centrosome, are involved in protein trafficking to and from the centrosome and centrosomal function, and regulate primary cilia. We show that Kif9 loss causes CS aggregation near the centrosome, leading to defects in cilia length and altering the levels of key primary cilia proteins like TALPID3, CEP131, CEP170, and CEP290.